Acute Rheumatic Fever and Rheumatic Heart Disease Essay

1875 Words 8 Pages
Introduction:
Acute Rheumatic Fever (ARF) and its successive partner, Rheumatic Heart Disease (RHD), pose a serious issue in paediatric health world wide. Alarmingly New Zealand is one of the biggest contributors and has the highest recorded number of ARF cases internationally (Jaine, Baker, & Venugopal, 2008). This essay will discuss the pathophysiology and epidemiology of ARF and RHD. It will focus on the impact this illness has on Maori and Pacific Island children in particular as ARF is almost exclusive within these ethnic groups (Atatoa-Carr, Bell, & Lennon, 2008; Sopoaga, Buckingham, & Paul, 2010). Additionally, the role that paramedics exhibit in acute cases of ARF will be discussed; with focus being on how paramedics and other
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In Australia there is a predominance of GAS Impetigo in those who contract ARF (Steer, & Carapetis, 2009) and according to Casey (2013)’s study there is low incidence of GAS pharyngitis within New Zealand, suggesting that other strains could also be effective causative agents. The signs and symptoms of ARF are migratory arthritis, arthalgia, fever, carditis, heart failure and chorea (Lennon, 2004). As RHD is the pathological development of ARF the relationship between the two is based upon the heart valve damage that occurs with each episode of ARF; with each recurrence of ARF causing greater damage (Jaine, Baker, & Venugopal, 2011). Therefore irreversible damage to the endocardium connective tissue, particularly the chordae tendinae, aortic and mitral valves results in RHD. The scarring from the inflammatory response affects valve leaflet elasticity causing them to become rigid and to fuse (valve stenosis). This results in the valves inability to carry out their normal purpose, leading to improper cardiac function (Porth, & Matfin, 2009). RHD takes different forms, in terms of its effect, dependant on the area of the heart that is most affected. When stenosis occurs in the aortic valve cardiac issues such as left ventricular hypertrophy, congestive heart failure, angina, and syncope due to decreased systolic ejection can develop (Gilbert, Wilson, & Finucane, 2011). Similarly if it is the

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